title: Leptospira interrogans serovar copenhageni harbors two lexA genes involved in SOS response.
abstract: Bacteria activate a regulatory network in response to the challenges imposed by DNA damage to genetic material, known as the SOS response. This system is regulated by the RecA recombinase and by the transcriptional repressor lexA. Leptospira interrogans is a pathogen capable of surviving in the environment for weeks, being exposed to a great variety of stress agents and yet retaining its ability to infect the host. This study aims to investigate the behavior of L. interrogans serovar Copenhageni after the stress induced by DNA damage. We show that L. interrogans serovar Copenhageni genome contains two genes encoding putative LexA proteins (lexA1 and lexA2) one of them being potentially acquired by lateral gene transfer. Both genes are induced after DNA damage, but the steady state levels of both LexA proteins drop, probably due to auto-proteolytic activity triggered in this condition. In addition, seven other genes were up-regulated following UV-C irradiation, recA, recN, dinP, and four genes encoding hypothetical proteins. This set of genes is potentially regulated by LexA1, as it showed binding to their promoter regions. All these regions contain degenerated sequences in relation to the previously described SOS box, TTTGN 5CAAA. On the other hand, LexA2 was able to bind to the palindrome TTGTAN10TACAA, found in its own promoter region, but not in the others. Therefore, the L. interrogans serovar Copenhageni SOS regulon may be even more complex, as a result of LexA1 and LexA2 binding to divergent motifs. New possibilities for DNA damage response in Leptospira are expected, with potential influence in other biological responses such as virulence.
authors.affiliation: Centro de Biotecnologia, Instituto Butantan, São Paulo, Brazil ; Departamento de Bioquímica, Instituto de Química, Universidade de São Paulo, São Paulo, Brazil.
authors.forename: Luciane S
authors.initials: LS
authors.lastname: Fonseca
authors.forename: Josefa B
authors.initials: JB
authors.lastname: da Silva
authors.forename: Juliana S
authors.initials: JS
authors.lastname: Milanez
authors.forename: Claudia B
authors.initials: CB
authors.lastname: Monteiro-Vitorello
authors.forename: Leonardo
authors.initials: L
authors.lastname: Momo
authors.forename: Zenaide M
authors.initials: ZM
authors.lastname: de Morais
authors.forename: Silvio A
authors.initials: SA
authors.lastname: Vasconcellos
authors.forename: Marilis V
authors.initials: MV
authors.lastname: Marques
authors.forename: Paulo L
authors.initials: PL
authors.lastname: Ho
authors.forename: Renata M A
authors.initials: RM
authors.lastname: da Costa
mesh_terms: D000595:Amino Acid Sequence; D001426:Bacterial Proteins / Q000737:chemistry / Q000235:genetics* / Q000378:metabolism*; D001665:Binding Sites; D004260:DNA Repair / Q000235:genetics; D018628:Gene Dosage; D015964:Gene Expression Regulation, Bacterial / Q000528:radiation effects; D023061:Gene Order; D016680:Genome, Bacterial; D007921:Leptospira interrogans / Q000145:classification / Q000235:genetics* / Q000378:metabolism* / Q000528:radiation effects; D008969:Molecular Sequence Data; D059372:Nucleotide Motifs; D016366:Open Reading Frames; D010641:Phenotype; D010802:Phylogeny; D011401:Promoter Regions, Genetic; D011485:Protein Binding; D013014:SOS Response, Genetics; D016415:Sequence Alignment; D012697:Serine Endopeptidases / Q000737:chemistry / Q000235:genetics* / Q000378:metabolism*; D014466:Ultraviolet Rays / Q000009:adverse effects; D000099160:LexA Repressor Protein
chemical_list: D001426:Bacterial Proteins; D012697:Serine Endopeptidases; D000099160:LexA Repressor Protein